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. 2021 May 29;21:632. doi: 10.1186/s12885-021-08388-1

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© The Author(s) 2021

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 5 — A ChIP-seq analysis reveals ChIP-seq peaks in the control (CTL) MiaPaCa-2 cells overlap significantly with MiaPaCa-2 cells over-expressing HDAC1 (red). An additional 17,501 peaks are identified with overexpression of HDAC1. B Cumulative distribution plot showing that HDAC1 binding sites identified upon overexpression of HDAC1 (blue) are nearby transcription start sites (TSS) of differentially expressed genes. C Scratch assay shows that overexpression of HDAC1 leads to increased migration compared to control cells. D Quantification of the scratch assays shows a significant difference with HDAC1 overexpression (Student’s T-test)